Alcohol addiction is a widespread problem in our society, yet initial exposure to alcohol does not universally result in addiction. The likely reason for this is varying levels of activity of an endogenous homeostatic mechanism which, when activated by alcohol consumption, reduces further consumption and thus prevents the development of addictive behaviors. The proposed research aims to further elucidate such a homeostatic pathway. Ethanol consumption triggers production of brain-derived neurotrophic factor (BDNF), and reduction of BDNF levels results in higher ethanol consumption. However, the downstream effectors of this ethanol-induced BDNF increase have not been determined. The proposed research will investigate the role of dynorphin, a protein which BDNF signaling can upregulate. First, the molecular connection between ethanol treatment and dynorphin production will be established. The link to ethanol-induced BDNF will be demonstrated both cellularly and behaviorally, by comparing wild type mice to conditional BDNF knockout mice. Finally, the proposed research will investigate the specific brain region in which this homeostasis occurs. These studies will increase our understanding of a brain mechanism for curbing alcohol addiction.